Background Although a rapid response system (RRS) can reduce the incidence of cardiopulmonary resuscitation (CPR) in general wards, avoidable CPR cases still occur. This study aimed to investigate the incidence and causes of avoidable CPR.
Methods We retrospectively reviewed the medical records of all adult patients who received CPR between April 2013 and March 2016 (35 months) at a tertiary teaching hospital where a part-time RRS was introduced in October 2012. Four experts reviewed all of the CPR cases and determined whether each event was avoidable.
Results A total of 192 CPR cases were identified, and the incidence of CPR was 0.190 per 1,000 patient admissions. Of these, 56 (29.2%) were considered potentially avoidable, with the most common cause being doctor error (n=32, 57.1%), followed by delayed do-not-resuscitate (DNR) placement (n=12, 21.4%) and procedural complications (n=5, 8.9%). The percentage of avoidable CPR was significantly lower in the RRS operating time group than in the RRS non-operating time group (20.7% vs. 35.5%; P=0.026). Among 44 avoidable CPR events (excluding cases related to DNR issues), the rapid response team intervened in only three cases (6.8%), and most of the avoidable CPR cases (65.9%) occurred during the non-operating time.
Conclusions A significant number of avoidable CPR events occurred with a well-functioning, part-time RRS in place. However, RRS operation does appear to lower the occurrence of avoidable CPR. Thus, it is necessary to extend RRS operation time and modify RRS activation criteria. Moreover, policy and cultural changes are needed prior to implementing a full-time RRS.
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Background Providing palliative care to dying patients in the intensive care unit (ICU) has recently received much attention. Evaluating the quality of dying and death (QODD) is important for appropriate comfort care in the ICU. This study aimed to validate the Korean version of the QODD questionnaire.
Methods This study included decedents in the ICUs of three tertiary teaching hospitals and one secondary hospital from June 2016 to May 2017. ICU staff members were asked to complete the translated QODD questionnaire and the visual analogue scale (VAS) questionnaire within 48 hours of patient death. The validation process consisted of evaluating construct validity, internal consistency, and interrater reliability.
Results We obtained 416 completed questionnaires describing 255 decedents. The QODD score was positively correlated with the 100-VAS score (Pearson correlation coefficient, 0.348; P<0.001). An evaluation of the internal consistency presented favorable results (calculated Cronbach’s alpha if a given item exceeded 0.8 in all items). The interrater reliability revealed no concordance between doctors and nurses.
Conclusions The QODD questionnaire was successfully translated and validated in Korean medical ICUs. We hope further studies that use this valuable instrument will be conducted in Korea.
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Background Arginine vasopressin (AVP) is widely used as a vasopressor agent. Some recent studies have suggested that AVP may exert an immunomodulatory effect. However, the mechanism about the anti-inflammatory effect of AVP is not well known. We investigated the effect of AVP on the ihibitor of kappa B (IκBα)/nuclear factor-kappa B (NF-κB) pathway in RAW 264.7 cells.
Methods Cultured RAW 264.7 cells were pretreated with AVP and stimulated with lipopolysaccharide (LPS). To evaluate the effect of AVP on inflammatory cytokines, the concentration of interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) were assessed by an enzyme-linked immunosorbent assay technique. The expression of IκBα and nuclear translocation of NF-κB p65 were measured by Western blotting, and IκB kinase (IKK) activity was analyzed by an in vitro immune complex kinase assay. To confirm the AVP effect on IκBα/NF-κB cascade and via V2 receptor, we added tolvaptan (V2 receptor antagonist) after AVP pretreatment.
Results The increase of IL-6 and TNF-α in LPS-stimulated RAW 264.7 cells was suppressed by a treatment with AVP. Pretreatment of AVP inhibited increasing of IKK activity and IκBα degradation induced by LPS in RAW 264.7 cells. Furthermore, LPS induced and NF-κB transcription was inhibited by AVP pretreatment. The observed changes in IKK activity, IκBα degradation and NF-κB transcription by AVP was abolished by tolvaptan treatment.
Conclusions Our results suggest that AVP showed anti-inflammatory effect on LPS-induced IκBα/NF-κB cascade in mouse macrophages via V2 receptors.
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